It is generally accepted that oral contraceptives may produce or enhance hypertension in some susceptible women. We have found similar enhancement in a strain of rats genetically predisposed to develop hypertension from a variety of noxious stimuli including chronic excess NaCl ingestion. Since oral contraceptives increase circulating angiotensin II the hypothesis that enhancement occurs by this means will be tested by studies utilizing a newly-developed specific competitive inhibitor of angiotensin II. An alternative hypothesis that enhancement is produced through sodium retention mediated by estrogen and/or angiotensin-stimulated aldosterone will be examined. Additionally, we have recently found a 64 percent prevalence of high blood pressure in the parents of a group of women in whom hypertension appeared to develop "de novo" during oral contraceptive therapy. Confirmation of the hypothesis that oral contraceptives cause the expression of a genetic locus or loci for hypertension to become more distinct at an early age will be sought by studying of female sibling pairs. The probands will be 200 women on oral contraceptives who have at least one female sibling of child-bearing age. Determination will be made of whether or not there is an excess of concordant relative to oral contraceptive therapy. Blood samples will be obtained for analysis for multiple polymorphic marker systems and linkage analysis.